[Medical aspects on sauna bathing]. / Bastubad kan vara bra vid ett antal sjukdomar ­ men fler studier krävs - Det vetenskapliga underlaget ännu inte tillräckligt för allmänna rekommendationer.

The literature describing medical aspects on sauna bathing is briefly reviewed. The circulatory effects of heating and subsequent cooling related to sauna bath differ with age, underlying medical condition and use of drugs. The circulatory changes may often be beneficial but can sometimes prove dangerous. More than 2000 sauna bathers were followed for around 20 years in a Finnish population study. The investigators have recently reported health benefits of abundant sauna use for individuals concerning hypertension, ischemic heart disease, dementia and certain pulmonary diseases. Others have recommended the use of sauna for patients with heart failure. Fatal events in sauna are very uncommon and often linked to the use of alcohol, to ischemic heart disease and to bathing alone. Medical conditions in which sauna bathing should be avoided are shortly reviewed. Further studies are urgently needed for illustration of the possible benefit of sauna bath at different medical conditions.

Atrial time and voltage dispersion are both needed to predict new-onset atrial fibrillation in ischemic stroke patients.

BACKGROUND: Atrial fibrillation (AF) is a known risk factor for ischemic stroke. Electrocardiographic predictors of AF in population studies such as the Framingham Heart Study, as well as in hypertensive patients have demonstrated a predictive value of the P-wave duration for development of AF. QRS vector magnitude has had a predictive value in ventricular arrhythmia development. We aimed to assess the value of the three-dimensional P-wave vector magnitude and its relationship to P-wave duration for prediction of new-onset AF after ischemic stroke. METHODS: First-ever ischemic stroke patients without AF at inclusion in the Lund Stroke Register were included. Measurements of P wave duration (Pd), QRS duration, corrected QT interval, and PQ interval were performed automatically using the University of Glasgow 12-lead ECG analysis algorithm. The P-wave vector magnitude (Pvm) was calculated automatically as the square root of the sum of the squared P-wave magnitudes in leads V6, II and one half of the P-wave amplitude in V2 ([Formula: see text]), based on the P-wave magnitude (Pvm) as defined by the visually transformed Kors' Quasi-orthogonal method. RESULTS: The median age was 73 (IQR 63-80) years at stroke onset (135 males, 92 females). Multivariate predictors of new-onset atrial fibrillation included age > 65 years, hypertension, and Pd/Pvm. A cut-off value of 870 ms/mV gave sensitivity, specificity, positive and negative predictive values of 51, 79, 30 and 87%, respectively. The Pd/Pvm was the only ECG predictor of AF with a significant multivariate hazard ratio of 2.02 (95% CI 1.18 to 3.46, p = 0.010). CONCLUSION: P-wave dispersion as measured by the Pd/Pvm was the only ECG parameter measured which independently predicted subsequent AF identification in a cohort of stroke patients. Further prospective studies in larger cohorts are needed to validate its clinical usefulness.

Ventricular repolarization sequences on the epicardium and endocardium. Monophasic action potential mapping in healthy pigs.

UNLABELLED: To investigate repolarization sequence, monophasic action potentials were recorded from a mean of 153 ± 54 left and right ventricular epicardial and endocardial sites in 10 pigs using the CARTO mapping system (Biosense Webster, Waterloo, Belgium). The activation time and end-of-repolarization (EOR) time were measured and 3-dimensional maps of activation and repolarization sequences constructed. RESULTS: In 8 of 9 pigs, both the activation and EOR times appeared first in the septum and last in the latero-basal areas on the endocardium, not on the epicardium. The EOR followed the activation sequence, both on the epicardium (in 8/9 pigs) and endocardium (in 8/8 pigs). The maximal EOR differences were 84 ± 20 ms, whereas the local EOR differences between paired sites against each other on the left ventricular epicardium and endocardium were 11 ± 9 ms in the apex and 12 ± 12 ms in the anterior wall. CONCLUSION: The EOR follows the activation sequence both on the epicardium and endocardium. The apico-basal gradients are predominant repolarization gradients, as compared with the epicardial-endocardial gradients.

Evolution of P-wave morphology in healthy individuals: a 3-year follow-up study.

BACKGROUND: Orthogonal P-wave morphology in healthy men and women has been described using unfiltered signal-averaged technique and holds information on interatrial conduction. The stability of P-wave morphology in healthy subjects over time is not fully known. METHODS: Sixty-seven healthy volunteers were investigated (29 males, aged 63 +/- 14 years, 48 females, 60 +/- 13 years). Orthogonal lead data (X, Y, and Z) were derived from standard 12-lead ECGs (recording length 6 minutes, sampling rate 1kHz, resolution 0.625 muV) recorded at baseline (BL), and 3 years later at follow-up (FU). P waves were then signal-averaged and analyzed regarding P-wave morphology, locations of maxima, minima, zero-crossings, and P-wave duration (PWD). RESULTS: No differences of P-wave variables were observed at FU compared to BL, including PWD (127 +/- 12 vs 125 +/- 14 ms at BL and FU, respectively, n.s.). In 59 of the 67 subjects (88%), the P-wave morphology was unaltered at FU. However, in the remaining eight cases a distinctively different morphology was observed. The most common change (P=0.030) was from negative polarity to biphasic (-/+) in Lead Z (n=5). In one case the opposite change was observed and in two cases transition into advanced interatrial block morphology was evident at FU. CONCLUSIONS: In the majority of healthy subjects, P-wave morphology is stable at 3-year FU. Subtle morphological changes, observed principally in Lead Z, suggest variation of interatrial conduction. These changes could not be detected by measuring conventional PWD that remained unchanged in the total population.

Pulmonary vein potentials in patients with and without atrial fibrillation.

BACKGROUND: Pulmonary vein (PV) potentials are invariably recordable at the PV ostia in patients with atrial fibrillation (AF) and delayed conduction around the PV ostia may play a role in the initiation and maintenance of AF. AIMS: To investigate the presence and extent of PV potentials in patients with and without AF. METHODS AND RESULTS: Circumferential catheter recordings at the PV ostia were obtained from 10 patients with paroxysmal AF and 9 with concealed Wolff-Parkinson-White (WPW) syndrome without history of AF. Typical PV potential was defined as either rapid deflections that separated from atrial deflection with a time delay in-between, or multiphasic, continuous or fractionated potentials. The presence of PV potentials was verified during sinus rhythm and during atrial pacing at the distal coronary sinus for the left PVs or at the right atrial appendage for the right PVs. To quantify the extent in which the PV potentials were recordable, the number of PVs with typical PV potentials recordable was counted. The time interval from the onset to the end of the electrograms recordable at the PV ostium (A-PV interval) was measured, and the maximal and mean of this interval were obtained. Typical PV potentials were recorded in 31 of 34 PVs (91%) in patients with AF, but in 4 of 36 PVs (11%) in patients with concealed WPW. A narrow, biphasic or triphasic, potential was recorded in 3 of 34 PVs (9%) in patients with AF, but in 29 of 36 (81%) PVs in patients with concealed WPW. The maximal and mean A-PV intervals were significantly longer in patients with AF (71 +/- 24 and 49 +/- 13 ms) than in patients with concealed WPW syndrome (33 +/- 14 and 25 +/- 6 ms). CONCLUSION: In patients with AF, typical PV potentials with marked conduction time delay were almost invariably recordable at the PV ostium, but in patients without a history of AF, merely simple, narrow potentials were found. These findings support the involvement of conduction delay and re-entrant activities around the PV ostia in the genesis and/or perpetuation of AF.

An algorithm for phase-space detection of the P characteristic points.

A new algorithm, based on embedding phase space, to detect the P-wave characteristic points of an ECG signal is reported in this paper. The multi-lead ECG is transformed into points of an embedding phase space where similar ECG morphologies are converted into phase space points that are close using some distance measure. The algorithm is robust with respect to the type of selected characteristic points (onset, peak and end), morphology changes, baseline oscillations and high frequency noise. The performance of the algorithm has been successfully validated using both simulated and real ECG signals.

Outcome parameters for trials in atrial fibrillation: executive summary.

Atrial fibrillation (AF), the most common atrial arrhythmia, has a complex aetiology and causes relevant morbidity and mortality due to different mechanisms, including but not limited to stroke, heart failure, and tachy- or bradyarrhythmia. Current therapeutic options (rate control, rhythm control, antithrombotic therapy, 'upstream therapy') only prevent a part of this burden of disease. Several new treatment modalities are therefore under evaluation in controlled trials. Given the multifold clinical consequences of AF, trials in AF patients should assess the effect of therapy in each of the main outcome domains. This paper describes an expert consensus of required outcome parameters in seven relevant outcome domains, namely death, stroke, symptoms and quality of life, rhythm, left ventricular function, cost, and emerging outcome parameters. In addition to these 'requirements' for outcome assessment in AF trials, further, more detailed outcome parameters are described. In addition to a careful selection of a relevant primary outcome parameter, coverage of outcomes in all major domains of AF-related morbidity and mortality is desirable for any clinical trial in AF.

Outcome parameters for trials in atrial fibrillation: recommendations from a consensus conference organized by the German Atrial Fibrillation Competence NETwork and the European Heart Rhythm Association.

Atrial fibrillation (AF), the most common atrial arrhythmia, has a complex aetiology and causes relevant morbidity and mortality due to different mechanisms, including but not limited to stroke, heart failure, and tachy- or bradyarrhythmia. Current therapeutic options (rate control, rhythm control, antithrombotic therapy, 'upstream therapy') only prevent a part of this burden of disease. New treatment modalities are therefore currently under evaluation in clinical trials. Given the multifold clinical consequences of AF, controlled trials in AF patients should assess the effect of therapy in each of the main outcome domains. This paper describes an expert consensus of required outcome parameters in seven relevant outcome domains, namely death, stroke, symptoms and quality of life, rhythm, left ventricular function, cost, and emerging outcome parameters. In addition to these 'requirements' for outcome assessment in AF trials, further outcome parameters are described in each outcome domain. In addition to a careful selection of a relevant primary outcome parameter, coverage of outcomes in all major domains of AF-related morbidity and mortality is desirable for any clinical trial in AF.

Age-related changes in P wave morphology in healthy subjects.

BACKGROUND: We have previously documented significant differences in orthogonal P wave morphology between patients with and without paroxysmal atrial fibrillation (PAF). However, there exists little data concerning normal P wave morphology. This study was aimed at exploring orthogonal P wave morphology and its variations in healthy subjects. METHODS: 120 healthy volunteers were included, evenly distributed in decades from 20-80 years of age; 60 men (age 50+/-17) and 60 women (50+/-16). Six-minute long 12-lead ECG registrations were acquired and transformed into orthogonal leads. Using a previously described P wave triggered P wave signal averaging method we were able to compare similarities and differences in P wave morphologies. RESULTS: Orthogonal P wave morphology in healthy individuals was predominately positive in Leads X and Y. In Lead Z, one third had negative morphology and two-thirds a biphasic one with a transition from negative to positive. The latter P wave morphology type was significantly more common after the age of 50 (P < 0.01). P wave duration (PWD) increased with age being slightly longer in subjects older than 50 (121+/-13 ms vs. 128+/-12 ms, P < 0.005). Minimal intraindividual variation of P wave morphology was observed. CONCLUSION: Changes of signal averaged orthogonal P wave morphology (biphasic signal in Lead Z), earlier reported in PAF patients, are common in healthy subjects and appear predominantly after the age of 50. Subtle age-related prolongation of PWD is unlikely to be sufficient as a sole explanation of this finding that is thought to represent interatrial conduction disturbances. To serve as future reference, P wave morphology parameters of the healthy subjects are provided.

Epicardial and endocardial dispersion of ventricular repolarization. A study of monophasic action potential mapping in healthy pigs.

OBJECTIVES: To investigate the total dispersion of ventricular repolarization of the epi- and endocardium. DESIGN: Monophasic action potentials (MAP) were recorded from 211+/-54 (151-353) left and right ventricular epi- and endocardial sites during atrial pacing in 10 pigs using the CARTO system. The activation time (AT), MAP duration (MAPd) and end of repolarization time (EOR) were measured. RESULTS: The total dispersion of AT, EOR and MAPd, defined as the maximal differences of these parameters over both the epi- and endocardium, were 57+/-10, 84+/-20, and 75+/-21 ms respectively and were significantly larger than the respective epi- and endocardial dispersions (p<0.05). The epicardial dispersion of AT, EOR and MAPd of both the right and left ventricles were significantly larger than that of each ventricle alone (p<0.02). Sternotomy did not affect these dispersion parameters. CONCLUSION: Detailed mapping of epicardial repolarization in vivo using the MAP mapping technique is feasible. Both the epi- and endocardium of the two ventricles contribute significantly to the total dispersion of repolarization.

Tpeak-Tend interval as an index of global dispersion of ventricular repolarization: evaluations using monophasic action potential mapping of the epi- and endocardium in swine.

UNLABELLED: The ECG interval from the peak to the end of the T wave (Tpeak-Tend) has been used as an index of transmural dispersion of ventricular repolarization (DVR). The correlation between the Tpeak-Tend interval and the global DVR, however, has not been well-evaluated. METHODS: Monophasic action potentials (MAPs) were recorded from 51+/-10 epicardial and 64 +/- 9 endocardial sites in the left ventricles of 10 pigs, and from 41+/-4 epicardial and 53+/-2 endocardial sites in the right ventricles of 2 of the 10 pigs using the CARTO mapping system. The end of repolarization times over the epi- and endocardium were measured, and the end of repolarization dispersions over the epicardium (DVR-epi), over the endocardium (DVR-endo) and over both (DVR-total) were calculated. The QTpeak, QTend and Tpeak-Tend intervals as well as the QTpeak and QTend dispersions were obtained from the simultaneously recorded 12-lead ECG. RESULTS: The maximal Tpeak-Tend intervals (57+/-7 ms) were consistent with the DVR-total (58+/-11 ms, p>0.05), and significantly correlated with the DVR-total (r=0.64, p<0.05). However, the mean Tpeak-Tend intervals (44+/-5 ms), and Tpeak-Tend intervals from lead II (41+/-6 ms) and V5 (43+/-5 ms) were all significantly smaller than and poorly correlated with the DVR-total, as were the QTpeak and QTend dispersions (15+/-2 ms vs. 21+/-4 ms). CONCLUSION: The maximal Tpeak-Tend interval may be used as a noninvasive estimate for the global DVR, but not the QTpeak and QTend dispersions, nor the mean Tpeak-Tend interval and that from a single lead.

Can orthogonal lead indicators of propensity to atrial fibrillation be accurately assessed from the 12-lead ECG?

AIMS: When analyzing P-wave morphology, the vectorcardiogram (VCG) has been shown useful to identify indicators of propensity to atrial fibrillation (AF). Since VCG is rarely used in the clinical routine, we wanted to investigate if these indicators could be accurately determined in VCG derived from standard 12-lead ECG (dVCG). METHODS: ECG and VCG recordings from 21 healthy subjects and 20 patients with a history of AF were studied. dVCG was calculated from ECG using the inverse Dower transform. Following signal averaging of P-waves, comparisons were made between VCG and dVCG, where three parameters characterizing signal shape and 15 parameters describing the P-wave morphology were used to assess the compatibility of the two recording techniques. The latter parameters were also used to compare the healthy and the AF groups. RESULTS: After transformation, P-wave shape was convincingly preserved. P-wave morphology parameters were consistent within the respective groups when comparing VCG and dVCG, with better preservation observed in the healthy group. CONCLUSION: VCG derived from routine 12-lead ECG may be a useful alternate method for studying orthogonal P-wave morphology.

In vivo validation of the coincidence of the peak and end of the T wave with full repolarization of the epicardium and endocardium in swine.

OBJECTIVES/BACKGROUND: Previous in vitro studies have suggested full repolarization of the epicardium coincides with the peak of the T wave (T(peak)) and that of the M cells coincides with the end of the T wave (T(end)). However, in vivo validation of the theory is lacking. METHODS: Monophasic action potentials (MAPs) were recorded using the CARTO mapping system from 51 +/- 10 epicardial sites and 64 +/- 9 endocardial sites of the left ventricle in 10 pigs and from 41 +/- 4 epicardial sites and 53 +/- 2 endocardial sites of the right ventricle in two of the 10 pigs. End of repolarization (EOR) times over the epicardium (EOR(epi)), endocardium (EOR(endo)), and over both (EOR(total)) were obtained. QT(peak) and QT(end) intervals were measured from simultaneously recorded 12-lead ECG. RESULTS: Minimal and maximal EOR(total) were observed in the left ventricle in all pigs. Minimal EOR(total) was on the epicardium in five pigs, and maximal EOR(total) was on the endocardium in nine pigs. Minimal, mean, and maximal QT(peak) intervals all were significantly smaller than maximal EOR(epi) (322 +/- 23 ms, P <.01). No significant difference was found between maximal QT(end) interval (338 +/- 30 ms) and maximal EOR(endo) (339 +/- 24 ms, difference = 1 +/- 19 ms, P =.92), between maximal QT(end) interval and maximal EOR(total) (341 +/- 24 ms, difference = 2 +/- 18 ms, P =.69), or between minimal QT(peak) interval (283 +/- 28 ms) and minimal EOR(total) (282 +/- 20 ms, difference = 0 +/- 15 ms, P =.95). CONCLUSIONS: In in vivo pig models, T(peak) does not coincide with full repolarization of the epicardium but coincides well with the earliest EOR, whereas the T(end) corresponds with the latest EOR. These findings suggest that not only the transmural gradients but also the apicobasal repolarization gradients contribute to genesis of the T wave.

Can pulsed ultrasound increase tissue damage during ischemia? A study of the effects of ultrasound on infarcted and non-infarcted myocardium in anesthetized pigs.

BACKGROUND: The same mechanisms by which ultrasound enhances thrombolysis are described in connection with non-beneficial effects of ultrasound. The present safety study was therefore designed to explore effects of beneficial ultrasound characteristics on the infarcted and non-infarcted myocardium. METHODS: In an open chest porcine model (n = 17), myocardial infarction was induced by ligating a coronary diagonal branch. Pulsed ultrasound of frequency 1 MHz and intensity 0.1 W/cm2 (ISATA) was applied during one hour to both infarcted and non-infarcted myocardial tissue. These ultrasound characteristics are similar to those used in studies of ultrasound enhanced thrombolysis. Using blinded assessment technique, myocardial damage was rated according to histopathological criteria. RESULTS: Infarcted myocardium exhibited a significant increase in damage score compared to non-infarcted myocardium: 6.2 +/- 2.0 vs. 4.3 +/- 1.5 (mean +/- standard deviation), (p = 0.004). In the infarcted myocardium, ultrasound exposure yielded a further significant increase of damage scores: 8.1 +/- 1.7 vs. 6.2 +/- 2.0 (p = 0.027). CONCLUSION: Our results suggest an instantaneous additive effect on the ischemic damage in myocardial tissue when exposed to ultrasound of stated characteristics. The ultimate damage degree remains to be clarified.

QT dispersion failed to estimate the global dispersion of ventricular repolarization measured using monophasic action potential mapping technique in swine and patients.

The aim of this study was to evaluate whether the QT dispersion measured from 12-lead electrocardiogram (ECG) can estimate the global dispersion of ventricular repolarization (DVR) measured using a monophasic action potential (MAP) mapping technique. Monophasic action potentials were recorded from 75 +/- 12 left ventricular sites in 10 pigs and from 48 +/- 16 left or right ventricular sites in 15 patients using the CARTO mapping system. The maximum DVRs in both end-of-repolarization and MAP duration among all the mapped sites were calculated and termed as global DVR for each measurement. QT intervals, QT peak and QT end , were measured from the 12-lead ECG, and QT dispersions; namely the differences between the maximum and the minimum of the QT peak and QT end were calculated. We found that QT dispersions were significantly smaller than (P < .05) and poorly correlated with the global DVRs both in pigs and patients. Bland-Altman agreement analysis demonstrated a marked variation of the differences and an obvious lack of agreement between the results obtained using the ECG and the MAP methods. In our patients, the global DVR increased markedly during ventricular tachycardia as compared with that during sinus rhythm (P < .05), whereas there was no significant difference in QT dispersion between these 2 subgroups. In conclusion, QT dispersion on the surface ECG could not estimate the global DVR measured using the MAP mapping technique. These findings are not consistent with some previously reported observations, suggesting the need for reappraisal of the electrophysiological implications of QT dispersion.

Activation recovery time measurements in evaluation of global sequence and dispersion of ventricular repolarization.

INTRODUCTION: Activation recovery time (ART), defined as the time from the earliest ventricular activation time to the end of T wave on unipolar electrograms, has been used as an index of myocardial repolarization time. However, it is unknown whether the ART can be used to estimate the global sequence and dispersion of ventricular repolarization as determined by the monophasic action potential (MAP) mapping technique. METHODS AND RESULTS: Endocardial MAPs and unipolar electrograms were simultaneously recorded using the CARTO system from 34 +/- 12 left (n = 6) or right (n = 9) ventricular sites in 12 patients. End-of-repolarization (EOR) times from the MAPs and ARTs from the unipolar electrograms were calculated, based on which 15 sets of 3-dimensional maps of global EOR sequence and ART sequence were reconstructed. The ART sequence was consistent with the EOR sequence in 14 of 15 maps. In the 473 paired measurements obtained, the differences between the ART and the EOR time were 2 +/- 22 milliseconds (NS). A significant positive correlation between the ART and the EOR time was found in all the maps (r = 0.58 +/- 0.22). Agreement analyses showed that the differences between these 2 measurements were almost all within the range of mean difference +/- 2 SD for each individual map and for all the 473 recordings. The global dispersion of ART was 79 +/- 35 milliseconds, as compared with that of EOR time of 78 +/- 35 milliseconds (NS). CONCLUSION: The ART from unipolar electrograms is a good estimate of EOR time measured from MAPs, suggesting the usefulness of the former in evaluation of global sequence and dispersion of ventricular repolarization.

Deterioration of interatrial conduction in patients with paroxysmal atrial fibrillation: electroanatomic mapping of the right atrium and coronary sinus.

OBJECTIVES: The purpose of this study was to analyze the velocities across the coronary sinus ostium (cross-CSo) and within the coronary sinus (intra-CS) in patients with and without paroxysmal atrial (AF) fibrillation and to estimate the interatrial conduction deterioration area in AF patients. BACKGROUND: Interatrial conduction delay in AF patients has been reported. However, localization of the interatrial conduction delay still is not clear. METHODS: Thirteen patients with paroxysmal AF and 10 control patients with AV nodal reentrant tachycardia or ectopic atrial tachycardia were enrolled in the study. Right atrial and CS mapping were performed using the CARTO electroanatomic mapping system during sinus rhythm and during distal CS pacing. The activation times and spatial distances of cross-CSo and intra-CS were measured between paired sites, from which the activation velocities of cross-CSo and intra-CS were obtained. RESULTS: During sinus rhythm, the activation velocities of cross-CSo in the AF group (1.2 +/- 0.2 m/s) were significantly slower than those in the control group (2.9 +/- 1.6 m/s, P < .05). During distal CS pacing, the cross-CSo velocities of the AF group (1.0 +/- 0.5 m/s) also appeared slower than those in the control group (1.4 +/- 0.2 m/s, P = .07). However, no difference was found in intra-CS activation velocities between the two groups (2.8 +/- 1.9 vs 3.2 +/- 2.2 m/s and 1.5 +/- 0.3 vs 1.4 +/- 0.3 m/s, P > .05 during sinus rhythm and distal CS pacing, respectively). CONCLUSIONS: Interatrial conduction at the posteroparaseptal region across the CS ostium was significantly slower in patients with paroxysmal AF than in control patients, further supporting the link between interatrial conduction deterioration and paroxysmal AF.

[Catheter ablation--new cure for paroxysmal atrial fibrillation. Case reports show how the trigger mechanism can be abolished]. / Kateterablation--ny bot vid paroxysmalt förmaksflimmer. Fallbeskrivningar visar hur själva triggerfaktorn kan slås ut.

The trigger mechanism of paroxysmal atrial fibrillation is usually an atrial ectopic beat originating in the muscular sleeves of the pulmonary veins. These and other origins of the trigger mechanisms can be explored with electroanatomical mapping technique. Once identified, the trigger mechanism may be abolished by using the catheter ablation technique to cure the arrhythmia. We present the results for two patients with trigger mechanisms of different origin whose arrhythmia has been cured using the focal ablation technique.

Five-year mortality for stable angina in a medical practice study and a randomized trial.

OBJECTIVE: Evolution of revascularization and medical therapy has increased the probability of improved survival in patients with stable angina. The present investigation tests the hypothesis that medical practice will generate lower mortality than randomly assigned bypass surgery in the European Coronary Surgery Study (ECSS) two decades earlier. METHOD: Using eligibility criteria of ECSS, a clinical decision strategy (CDS) cohort of 362 patients was selected from a nationwide study of medical practice in Sweden. Access to the individual data allowed common protocol design to compare 5-year mortality between CDS and surgical strategy of ECSS. RESULTS AND INTERPRETATION: CDS advised bypass surgery (BS) or percutaneous transluminal coronary angioplasty (PTCA) in 93% and medical treatment alone in 7%, while 94% of 394 patients randomized to surgery (Euro-S) in ECSS obtained BS. Operative mortality was 3.2% for Euro-S while no operative deaths occurred in CDS reflecting medical progress during two decades. However, the 5-year mortality for CDS decreased first when the risk ratio was adjusted for age, diabetes mellitus and hypertension (RR = 0.49 with 95% CI 0.26-0.93) p = 0.03 suggesting a need for improved comprehensive medical care.